Abstract

Allograft inflammatory factor-1 (AIF-1) is a cytoplasmic protein that is encoded by the AIF1 gene. The main functions of AIF-1 are the activation of macrophages and enhancing the production of pro-inflammatory cytokines. To date, three different AIF-1 isoforms have been identified. In this study, we examined the expression of AIF-1 isoforms on the level of mRNA, and we compared the percentage of AIF-1-positive white blood cells (WBCs) in blood and AIF-1/CD68 cells in the synovial membranes in patients with rheumatoid arthritis (RA) and osteoarthritis (OA). We examined 15 patients with RA and 15 patients with OA who had previously undergone knee arthroplasty. Peripheral blood and synovial membranes (SMs) were collected from these patients during knee arthroplasty. We identified three AIF-1 mRNA expression variants in peripheral mononuclear cells (PBMCs) and SMs from patients in both groups. Spearman’s rank correlation coefficient tests showed strong, positive, and significant correlations between the three AIF-1 mRNA expression variants in PBMCs and/or SMs in patients with RA and OA. There were no statistically significant correlations for any of the AIF-1 mRNA expression variants between PBMCs and SMs in patients with RA and OA. We observed a statistically significant increased percentage of AIF-1-positive cells in patients with RA in comparison to patients with OA. The percentage of AIF-1-positive cells in the blood of patients with RA and OA was 1.35 ± 0.81% and 0.71 ± 0.25% (p < 0.01), respectively, whereas the percentage of AIF-1/CD68-positive WBC cells in the SMs was 24.05 ± 7.17% and 4.78 ± 1.52% (p < 0.001), respectively. In conclusion, three AIF-1 mRNA expression variants occurred in PBMCs and SM cells in patients with RA and OA. The AIF-1 mRNA expression levels of the variants correlated with each other in PBMCs and SM cells, but there were no statistically significant correlations for AIF-1 mRNA expression variants between PBMCs and SM cells in patients with RA and OA. Both in the blood and SMs, we observed an increased percentage of AIF-1-positive cells in patients with RA in comparison to patients with OA. The above results suggested that AIF-1 was the cytokine involved in the pathogenesis of RA. The precise knowledge of the role of AIF-1 in RA pathogenesis and the development of inflammatory response requires further investigations.

Highlights

  • Rheumatoid arthritis (RA) is a chronic autoimmune disease, resulting in joint damage and functional disability

  • We examined the expression of Allograft inflammatory factor-1 (AIF-1) isoforms on the level of mRNA, and we compared the percentage of AIF-1-positive cells in patients with RA and OA

  • In peripheral blood mononuclear cells (PBMCs) fractions, we detected the lowest expression in the v.4 transcript and highest expression in the v.1 transcript in both groups; there were no statistically significant differences between the patient groups

Read more

Summary

Introduction

Rheumatoid arthritis (RA) is a chronic autoimmune disease, resulting in joint damage and functional disability. AIF-1 is one of the factors responsible for inflammation in RA [15,16] In this disease, AIF-1 is detected in peripheral blood mononuclear cells (PBMCs), monocytes, and macrophages in synovial membranes (SMs) [17]. In patients with breast cancer, the expression of AIF-1 isoforms (variants) has been observed in breast adipose tissue monocytes and M1 macrophages. Previous studies have shown increased expression of AIF-1 protein or AIF-1-positive cells in RA patients. We indicated an increased number of AIF-1-positive cells in the blood and SMs from patients with RA [17]. We examined the expression of AIF-1 isoforms on the level of mRNA, and we compared the percentage of AIF-1-positive cells in patients with RA and OA

Patients
Quantitative Real-Time Polymerase Chain Reaction
Flow Cytometry
Immunofluorescence Analysis of Synovial Samples
Statistical Analysis
Expression of AIF-1 Isoforms in PBMCs and SMs in Patients with RA and OA
Correlations of AIF-1 Variant mRNA Expression
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call